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10.1016/j.molcel.2016.10.021 http://scihub22266oqcxt.onion/10.1016/j.molcel.2016.10.021 C5340194!5340194!27889452     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cell 2016 ; 64 (6): 1074-87 Nephropedia Template TP {{tp|p=27889452|t=2016. An RB-EZH2 Complex Mediates Silencing of Repetitive DNA Sequences |pdf=|usr=}}{{27889452}} gab.com Text An RB-EZH2 Complex Mediates Silencing of Repetitive DNA Sequences JO: Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=27889452 #FOAvip Repetitive genomic regions include tandem sequence repeats and interspersed repeats, such as endogenous retroviruses and LINE-1 elements. Repressive heterochromatin domains silence expression of these sequences through mechanisms that remain poorly understood. Here, we present evidence that the retinoblastoma protein (pRB) utilizes a cell-cycle-independent interaction with E2F1 to recruit enhancer of zeste homolog 2 (EZH2) to diverse repeat sequences. These include simple repeats, satellites, LINEs, and endogenous retroviruses as well as transposon fragments. We generated a mutant mouse strain carrying an F832A mutation in Rb1 that is defective for recruitment to repetitive sequences. Loss of pRB-EZH2 complexes from repeats disperses H3K27me3 from these genomic locations and permits repeat expression. Consistent with maintenance of H3K27me3 at the Hox clusters, these mice are developmentally normal. However, susceptibility to lymphoma suggests that pRB-EZH2 recruitment to repetitive elements may be cancer relevant. Twit Text FOAVip An RB-EZH2 Complex Mediates Silencing of Repetitive DNA Sequences ????Mol Cell http://www.kidney.de/pget.php?&tw=1&pmid=27889452 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27889452 #FOAvip English Wikipedia <ref>{{Cite pmid|27889452}}</ref> An RB-EZH2 Complex Mediates Silencing of Repetitive DNA Sequences #MMPMID27889452 Ishak CA; Marshall AE; Passos DT; White CR; Kim SJ; Cecchini MJ; Ferwati S; MacDonald WA; Howlett CJ; Welch ID; Rubin SM; Mann MR; Dick FA Mol Cell 2016[Dec]; 64 (6): 1074-87 PMID27889452show ga Repetitive genomic regions include tandem sequence repeats and interspersed repeats, such as endogenous retroviruses and LINE-1 elements. Repressive heterochromatin domains silence expression of these sequences through mechanisms that remain poorly understood. Here, we present evidence that the retinoblastoma protein (pRB) utilizes a cell-cycle-independent interaction with E2F1 to recruit enhancer of zeste homolog 2 (EZH2) to diverse repeat sequences. These include simple repeats, satellites, LINEs, and endogenous retroviruses as well as transposon fragments. We generated a mutant mouse strain carrying an F832A mutation in Rb1 that is defective for recruitment to repetitive sequences. Loss of pRB-EZH2 complexes from repeats disperses H3K27me3 from these genomic locations and permits repeat expression. Consistent with maintenance of H3K27me3 at the Hox clusters, these mice are developmentally normal. However, susceptibility to lymphoma suggests that pRB-EZH2 recruitment to repetitive elements may be cancer relevant. äAn RB-EZH2 Complex Mediates Silencing of Repetitive DNA Sequences (epmc).pdf DeepDyve Pubget Overpricing